Abstract
Hyperhomocysteinemia is a well-known risk factor for atherosclerosis, coronary heart disease, stroke, and venous thrombosis. However, in recent decades, the range of diseases associated with elevated homocysteine levels has expanded significantly. The influence of this amino acid on the occurrence and development of pathologies of the respiratory system, in particular, chronic obstructive pulmonary disease, bronchial asthma, lung and pleural cancer, is currently being actively studied. The aim of the study is to find the features of histological changes in the lungs of adult rats under conditions of hyperhomocysteinemia. The experimental study was performed on 22 white nonlinear adult (6-8 months) male rats. During the experiment, the animals were divided into two groups – control and experimental. Simulation of the state of persistent hyperhomocysteinemia was achieved by administering to rats the experimental group of thiolactone homocysteine at a dose of 200 mg/kg body weight intragastrally for 60 days. Histological specimens were studied using an SEO CCAN light microscope and photo-documented using a Vision CCD Camera with an image output system from histological specimens. Histological examinations of the lungs of adult animals under conditions of hyperhomocysteinemia revealed adaptive-compensatory and destructive changes in the components of the organ. Discirculatory disorders, remodeling of the bronchial wall with the formation of inflammatory infiltrates in them were revealed. Significant areas of dys- and atelectasis and emphysematically altered areas of the parenchyma were found in the respiratory tract of the lungs. In the alveolar septa, peribronchially and paravasally, histo- and leukocyte infiltration, formation of inflammatory conglomerates were determined. Remodeling of vascular walls, especially the microcirculatory tract leads to disruption of blood supply to the body and hypoperfusion of lung tissue.
Highlights
Respiratory diseases today are extremely common among children and adults
There is some evidence in the scientific literature on the involvement of endothelial dysfunction in the occurrence and progression of respiratory diseases
The latter differ in the causes and mechanisms of development, but the potential factors of endothelial damage in each of them are universal, namely: focal or diffuse inflammation of bronchopulmonary tissue, disorders of free radical oxidation, hypoxia, proteinase imbalance, neurohumoral dysfunction [2, 6, 10, 18]
Summary
Respiratory diseases today are extremely common among children and adults. The reasons for their development are polyetiological and are being actively studied. There is some evidence in the scientific literature on the involvement of endothelial dysfunction in the occurrence and progression of respiratory diseases The latter differ in the causes and mechanisms of development, but the potential factors of endothelial damage in each of them are universal, namely: focal or diffuse inflammation of bronchopulmonary tissue, disorders of free radical oxidation, hypoxia, proteinase imbalance, neurohumoral dysfunction [2, 6, 10, 18]. The main triggers that can activate the mechanisms of endothelial damage are cytokines, bacterial toxins, pollutants of tobacco smoke, immune complexes, free radicals, and so on. These factors are well known and have a significant evidence base. The increase in its content in the blood is accompanied by a number of negative changes in organs and systems, one of which is endothelial
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